Eun Kyung Lee receieved her Ph.D. in Molecular and Cellular Biology from Gwangju Institute of Science and Technology (GIST), South Korea in 2006. She has completed postdoctoral training at Johns Hopkins Medical Institutes and National Institutes of Health/National Institute on Aging (NIH/NIA), USA from 2007 to 2011. She is an assistant professor at Catholic University of Korea, College of Medicine since 2011. Her research interests are focused to RNA metabolism between health and diseases including cancer. Her group studies molecular mechanisms of RNA regulation by RNA binding proteins or non-coding RNAs in mammalian models of tumorigenesis, epithelial-mesenchymal transition, and senescence
p130Cas regulates cell adhesion and migration by mediating tyrosine receptor kinase signaling. Tight regulation of p130Cas expression is critical for the maintenance of cell motility, survival and apoptosis in various cell types. Several studies reveal that transcriptional and post-translational control of p130Cas is important to maintain its expression and activity. To explore novel regulatory mechanisms for p130Cas expression, we investigated the effect of microRNAs on p130Cas level in human breast cancer cells. Here, we provide experimental evidences that miR-329 is a novel factor regulating p130Cas expression. miR-329 down-regulates cell migration and invasion thereby suppress tumor growth via down-regulating p130Cas. Ectopic expression of p130Cas restored the inhibitory effects of miR-329 in tumor progression. Interestingly, relative expression of miR-329 and p130Cas is inversely correlated between normal and breast cancers; miR-329 decreased, while p130Cas increased in breast cancers. Taken together, our results suggest that miR-329 is a novel factor regulating p130Cas expression and aberrant expression of p130Cas is responsible for tumor progression in breast cancers.
Soon-Sun Hong is a professor in the Translational Research Center, Department of Biomedical Sciences, at the Inha University, South Korea.
Crizotinib, a c-MET/ALK inhibitor, has exhibited antitumor efficacy in different types of cancers. However, studies regarding Crizotinib in pancreatic cancer have been limited. Thus, we investigated the effect of Crizotinib on pancreatic cancer and its mechanism of action. Crizotinib strongly suppressed the growth and proliferation of pancreatic cancer cells in a dose-dependent manner. Also, it induced apoptosis by modulating its related factors. In the study, with regard to the mechanism of action, Crizotinib did not inhibit c-MET expression on pancreatic cancer cells; instead, it specifically inhibited the activity of ALK, which was identified to be highly expressed on various pancreatic cancer cells and tissues in our study. In 42 different receptor tyrosine kinase (RTKs) array, Crizotinib also strongly inhibited the expression of activated ALK in pancreatic cancer cells, modulating its downstream mediators such as STAT3, AKT, and ERK. Furthermore, Crizotinib inhibited angiogenesis in a mouse Matrigel plug assay as well as the progression of tumor growth in a mouse xenograft model. Taken together, our investigation shows that Crizotinib inhibits the ALK signaling pathway in pancreatic cancer, resulting in cell growth/angiogenesis inhibition and apoptosis induction. We suggest that Crizotinib might be used as a novel therapeutic drug for treating pancreatic cancer.